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IGF1 — JAK2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: JAK2 → Complex of IGF1-IGF1R (increases) Zong et al., J Biol Chem 2000*
  Evidence: We found that STAT3, but not STAT5, was activated in response to IGF-I in 293T cells cotransfected with IGF-IR and STAT expression vectors. Moreover, tyrosine phosphorylation of STAT3, JAK1, and JAK2 was increased upon IGF-I stimulation of endogenous IGF-IR in 293T cells transfected with the respective STAT or JAK expression vector.

Text-mined interactions from Literome

Takahashi et al., Circ Res 1999 : These results indicated that ( 1 ) IGF-1 activated JAK1 but not JAK2 or Tyk2 in rat cardiomyocytes ; ( 2 ) IGF-1 induced both tyrosine and serine phosphorylation of STAT1 and STAT3 ; and ( 3 ) the tyrosine phosphorylation of STAT3 was not caused by JAK1 alone, and protein kinase C and intracellular Ca ( 2+ ) were required for phosphorylation
Ray et al., Int J Oncol 2007 (Breast Neoplasms...) : MCF-7 cells expressed higher levels of Ob-Rb, Jak2 , PI3K, Stat3 and p-Stat3 in a dose dependent manner to 50 ng/ml at 24 h ; and IGF-IRalpha increased at 24 h. Cyclin D1 and Cox-2 levels increased with leptin treatment
Gual et al., Endocrinology 1998 : Taking our data together, we conclude that : 1 ) insulin and IGF-1 lead to phosphorylation and activation of JAK-1 and JAK-2 in intact cells ; 2 ) phosphorylation of IRS-I by JAK-1 seems to occur on sites different from those phosphorylated by the insulin receptor ; 3 ) JAK-1 interacts directly with phosphorylated insulin and IGF-1 receptors ; and 4 ) the JH7-JH6 and JH1 domains of JAK-1 are responsible for the interaction with insulin and IGF-1 receptors